Summary of Work: The purpose of this project is to examine the neurophysiological control of laryngeal movement for speech and swallowing in normal individuals and individuals with laryngeal movement disorders. Studies addressed the role of sensory input in laryngeal motor control for volitional activities such as phonation for speech, airway protection and swallowing. Basic studies have examined whether laryngeal sensory stimulation induced neuronal activity in the periaqueductal gray (PAG), a midbrain region known to be involved in vocalization in mammals. We determined the number of neurons expressing Fos, the protein product of the immediate early gene c-Fos in the PAG after electrical stimulation of the internal branch of the superior laryngeal nerve in experimental and control animals. Discrete areas of the PAG well known to be involved in vocalization were found to have the greatest numbers of Fos-expressing neurons in the experimental animals. To examine the role of sensation during laryngeal control for speech and swallow, two studies were completed in normal volunteers. The laryngeal adductor reflex, which can be elicited by stimulation of the superior laryngeal nerve (SLN) and is thought to have a role in airway protection, was studied during different phases of swallowing in normal volunteers. It was hypothesized that this reflex mechanism would be particularly active during the swallow when airway protection has functional importance. The SLN was stimulated at different times: on initiation of the swallow; during the swallow; and between 3 and 5 seconds after completion of the swallow. Unexpectedly, the later response, the R2 which occurs bilaterally between 65 and 75 ms after SLN stimulation was suppressed during the swallow and for 3 seconds after swallowing. In contrast, the earlier R1 response was unaffected by swallowing activity. This suggests that laryngeal protective brain stem mechanisms continue to be active during swallowing while later more central responses elicited by sensory stimulation may be suppressed. The role of sensation during speech and while holding one's breath was also examined in normal volunteers. During both of these volitional control tasks, the frequency and amplitude of the early R1 brainstem response were suppressed as were the later R2 bilateral responses. Thus volitional laryngeal motor control usually suppresses protective airway reflexes. We have also continued our studies of laryngeal sensory-motor functioning in individuals with motor control disorders. Previously we demonstrated that laryngeal sensori-motor reflex responses are suppressed during reflex response conditioning with continued stimulation at precise intervals in normal volunteers. Such reflex responses were not similarly suppressed in individuals with adductor spasmodic dysphonia. The results suggested that a reduction in the normal sensori-motor response suppression mechanisms may play a role in the pathophysiology of adductor spasmodic dysphonia. To examine whether this was specific to adductor spasmodic dysphonia, studies on two additional patient groups were completed this year: persons with abductor spasmodic dysphonia, and individuals with vocal tremor. The abnormalities found in individuals with abductor spasmodic dysphonia were similar to those found in persons with adductor spasmodic dysphonia, while individuals with vocal tremor did not have laryngeal sensori-motor response conditioning abnormalities. Thus the pathophysiology involved in spasmodic dysphonia was found to differ from that involved in vocal tremor. This project will be terminated and replaced by study of sensory function in laryngeal disorders.